Peak creatine kinase as a measure of effectiveness of thrombolytic therapy in acute myocardial infarction.

As part of the National Heart, Lung, and Blood Institute multicenter Thrombolysis in Myocardial Infarction Trial, the time to peak plasma creatine kinase (CK) activity as a marker of reperfusion in 272 patients with validated acute myocardial infarction was analyzed. Patients were treated with either tissue-type plasminogen activator or streptokinase by intravenous administration. All patients underwent acute coronary angiography. The infarct-related artery was identified and thrombolytic therapy administered. Reperfusion at 90 minutes was documented by angiography. CK was determined before institution of therapy and every 4 hours thereafter for the first 24 hours. Patients were classified into 3 groups for comparative purposes: group 1--occlusion with no reperfusion (n = 119); group 2--occlusion with reperfusion (n = 98); and group 3--subtotal occlusion (n = 55). Early (within 4 hours after treatment) and late (more than 16 hours after treatment) peaking of CK differentiated patients with drug-induced perfusion from those without reperfusion. Although peak CK between 5 and 11 hours after drug treatment did suggest perfusion through the infarct-related artery, it did not differentiate between drug-induced and spontaneous reperfusion. Clinically, early peak CK is a useful noninvasive means of assessing coronary artery patency. However, in clinical trials assessing drug therapy, the use of peak CK may overestimate drug effectiveness by including patients with spontaneous reperfusion.